We are continuing our studies on factors which control the migration and proliferation of connective tissue cells. We have shown that the platelet-derived growth factor (PDGF) appears to function as a wound hormone. PDGF is normally released at sites of trauma during platelet-aggregation, where it acts as a potent chemoattractant for connective tissue cells. In concert with other peptide growth factors, PDGF stimulates the division of these cells. In vivo studies indicate that addition of PDGF to wounds can accelerate the rate of new tissue formation in both normal as well as wound repair impaired animals. In order to better characterize the role of PDGF in wound repair we have investigated animals models with decreased levels of circulating platelets, such as animals undergoing chemotherapy with adriamycin. In these studies we showed that treatment of animals with adriamycan prior to wounding caused an 80% reduction in the amount of new tissue formed at the wound site while treatment during the time of repair had no inhibitory effect. This indicates that adriamycin impairs wound repair via an indirect mechanism, possible by decreasing the levels of PDGF and other wound signals produced immediately at the time of wounding which are essential for the initiation of the repair process. Related studies indicate that there are specific factors for each cell type which participates in the repair process. We are presently involved in the characterization and isolation of chemotactic factors for endothelial cells and skin epidermal cells which are present at wound sites. These factors might be used to augment the levels normally present in various wounds and accelerate the rate of repair.